Supplemental information for: Inhibition of CSF1R and KIT with pexidartinib reduces inflammatory signaling and cell viability in endometriosis

Endometriosis is a common and debilitating disease, affecting ~170 million women worldwide. Affected patients have limited therapeutic options such as hormonal suppression or surgical excision of the lesions, though therapies are often not completely curative. Targeting receptor tyrosine-kinases (RTKs) could provide a nonhormonal treatment option for endometriosis. We determined that two RTKs, Macrophage colony stimulating factor receptor (CSF1R) and Mast/stem cell growth factor receptor KIT (KIT), are overexpressed in endometriotic lesions and could be novel nonhormonal therapeutic targets for endometriosis. The kinase activity of CSF1R and KIT is suppressed by pexidartinib, a small molecule inhibitor that was recently approved by the US Food and Drug Administration (FDA). Using immunohistochemistry, we detected CSF1R and KIT in endometriotic tissues obtained from peritoneal lesions, colorectal lesions, and endometriomas. Specifically, we show that KIT is localized to the epithelium of..., , , # Supplemental Information for \"Inhibition of CSF1R and KIT with pexidartinib reduces inflammatory signaling and cell viability in endometriosis\"

## Description of the data and file structure

The data provided here is supplemental information derived from the investigative work that led to the primary manuscript. First, work with immunohistochemistry shows the relationship of expression patterns in the protein CSF1R and the macrophage marker, CD68. The following western blots describe dose-response assays using protein phosphorylation in immortalized endometriosis cells (12Z) to assess for upregulation of CSF1R and KIT signaling when exposed to their respective ligands. Next, western blots of control experiments are shown evaluating if pexidartinib is able to reduce protein phosphorylation independent of cell exposure to ligand stimulation. Additional control experiments show the results of gene expression when 12Z cells were exposed to pexidartinib without stimulatory ligands to as...

子宫内膜异位症（Endometriosis）是一种常见且可导致严重功能障碍的疾病，全球约有1.7亿女性受其困扰。患者的临床治疗选择十分有限，仅可采用激素抑制疗法或手术切除异位病灶，但此类方案往往无法实现完全治愈。靶向受体酪氨酸激酶（receptor tyrosine-kinase, RTKs）有望为子宫内膜异位症提供非激素治疗新策略。本研究证实，两种受体酪氨酸激酶——巨噬细胞集落刺激因子受体（Macrophage colony stimulating factor receptor, CSF1R）与肥大细胞/干细胞生长因子受体KIT（Mast/stem cell growth factor receptor KIT, KIT）在子宫内膜异位病灶中呈过表达状态，可作为该疾病新型非激素治疗靶点。美国食品药品监督管理局（US Food and Drug Administration, FDA）近期批准的小分子抑制剂普沙替尼（pexidartinib）可有效抑制CSF1R与KIT的激酶活性。本研究通过免疫组织化学技术，在腹膜异位病灶、结直肠异位病灶及子宫内膜异位囊肿（endometriomas）的组织样本中均检测到了CSF1R与KIT的表达。具体而言，本研究证实KIT定位于……。
# 《使用普沙替尼抑制CSF1R与KIT可降低子宫内膜异位症中的炎症信号通路活性与细胞活力》补充信息

## 数据与文件结构说明
本数据集提供的补充信息源自支撑该主手稿的研究工作。首先，免疫组织化学实验结果展示了蛋白质CSF1R与巨噬细胞标志物CD68的表达模式相关性。后续的蛋白质免疫印迹实验描述了以永生化子宫内膜异位症细胞株12Z的蛋白质磷酸化水平为检测指标的剂量响应试验，用于评估在暴露于相应配体时，CSF1R与KIT信号通路的上调情况。随后展示了对照实验的蛋白质免疫印迹结果，旨在评估普沙替尼是否可在细胞未接受配体刺激的前提下降低蛋白质磷酸化水平。额外的对照实验则展示了12Z细胞在未受刺激性配体刺激、仅暴露于普沙替尼时的基因表达结果……。